By Gary C. Kanel
The Atlas of Liver Pathology, via Drs. Gary C. Kanel and Jacob Korula, offers the visible information you want to safely diagnose all kinds of liver affliction. equipped via ailment kind, it issues out significant histological positive factors, updates sickness parameters with new pictures and diagrams, and is helping you already know the medical facets of every affliction. It presents quickly and handy connection with nearly all the liver problems typically obvious at the present time. Nine-hundred-plus high quality, full-color pictures catch the gross and histological presentation of liver pathology excellent for comparability to the specimens you stumble upon in perform.
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Overall, biopsies are usually not useful to predict recovery. 8. A number of pathophysiologic processes play a role and include the following: a. Immune-mediated injury (most important with HBV infection; fulminant hepatitis often occurs in the absence of detectable HBV because of the low level of viral replication) b. Injury from activation of cytokines, tumor necrosis factor (TNF), and interleukins (IL-1 and IL-6) c. Tissue hypoxia (decreased hepatic perfusion secondary to disturbance in the microvasculature; capillary obstruction from debris such as actin filaments and collagen) e.
Hepatitis G virus (HGV) i. In general, the portal and lobular inflammation and the lobular necrosis are milder than what is seen with the other hepatotropic viruses. ii. There is some question whether acute HGV infection does, in fact, cause a histologically apparent acute hepatitis, with many believing it is more a passenger virus. Figure 2-6 Acute viral hepatitis, apoptosis. A, Diffuse necroinflammatory changes are seen, with spotty necrosis and hypertrophic Kupffer cells. Toward the left of the field, occasional hepatocytes show a more intense eosinophilic cytoplasm with smaller pyknotic nuclei (apoptosis).
Figure 2-30 Chronic viral hepatitis. Nuclear anisocytosis and mild fatty change are seen. Figure 2-33 Chronic viral hepatitis: hepatitis B virus (HBV) + δ. The degree of lobular necroinflammatory activity can sometimes be diffuse and is often seen in chronic HBV with associated δ virus infection, as this example demonstrates. 2. Lobular necrosis, inflammation, hydropic change, and apoptosis away from the periportal zones occur and are often irregularly distributed from one lobule to the next. 3.